Neurofeedback For Autistic Spectrum Disorders: Promising Results In A Small Sample

Autistic Spectrum Disorders (ASD) are characterized by significant deficits in social skills, attention/concentration, and communication, as well as emotional, cognitive, and behavioral impairments. Examples include Autism, Asperger’s Disorder, and Pervasive Developmental Disorder Not Otherwise Specified. I am not aware of any treatment that can “cure” ASD. Current therapies focus on symptom reduction, behavioral and social skills training, and quality of life enhancements.

Kouijzer et al. (2009)* investigated the effects of neurofeedback in a group of 12 male and 2 female children (ages 8-12 years with a average age of 10.1) diagnosed with Pervasive Developmental Disorder, Not Otherwise Specified. Seven of 14 participants underwent neurofeedback training (“experimental group”), while the remaining persons received no treatment (“wait-list control group” or just “control group”). Experimental groups are often compared to control groups in research to help control for experimental confounds (variables that can seriously jeopardize the results of study), placebo effects (the effects of participants belief that their health will improve even if given a sham treatment), and to determine the magnitude of a treatment. A non-randomized, pre-test/post-test design (the same set of tests were given before and after the experiment) was used. Wait-list control and experimental participants were “matched.” Matched designs attempt to make comparisons between subjects who are judged to be more or less equivalent in the variables under investigation. For example, an experimenter might “match” subjects with similar levels of depression when testing a new anti-depressant so that the actual effects of the drug can more accurately estimated.

This part gets a little more technical. Based on previous research, Kouijzer et al. developed an argument that neurofeedback might improve abnormal theta-to-beta ratios in persons with ASD. Specifically, the researchers hypothesized that a classic neurofeedback protocol called “SMR training” (inhibit frequencies less than 10Hz and enhance 12-15 Hz [often called “low beta” or “SMR”] along the cerebral motor strip using a 2 channel, C3/C4 protocol), might improve executive functioning (attention/concentration, mental flexibility, speed and efficiency, and goal setting) and communication abilities. (NOTE: see an updated on the protocol used in this study in the comments section below). Don’t worry about the frequency bands and names – just know that specific electrical energy of the brain was either enhanced or inhibited. The researchers reasoned and cited existing evidence that SMR training activates an important region of the brain called the anterior cingulate cortex that is responsible for cognitive and emotional regulation (a deficit in Autistic Spectrum Disorders). It is worth noting that elevated theta-to-beta ratios can occur in and are believed by some to be a defining feature of the EEG in attention deficit hyperactivity disorder (ADHD).

Outcome measures included executive, social, and neurophysiological (QEEG) levels of functioning. All persons in the experimental group received 40 neurofeedback sessions (this is a fairly average amount of sessions in my experience). The researchers reported impressive results following the completion of neurotherapy. Experimental group participants realized statistically significant improvements in the following areas: sustained auditory selective attention (30%), inhibition of verbal responses (55%), inhibition of motor responses (15%), set shifting (57%), concept generalization (50%), and planning ability (37%). Significant improvements were also found in communication (17%), general communication (14%), social interaction (16%), and typical behavior (9%). Percentages reflect improvement in the experimental group at their post-assessment compared to their pre-assessment.

No statistically significant improvements were found in areas of verbal and visual memory and sustained attention; however, the authors’ noted that many of the participants did not exhibit deficits in these areas at the start of the study. Additionally, the post-QEEG (brainmap) did not show statistically meaningful changes when compared to the control group despite obvious treatment benefits. A current debate exists in the field regarding pre-post QEEGs and the factors that can account for changes or lack thereof. This is a highly technical discussion that I will not address in this report.

The fact that Kouijzer et al. obtained significant results with a relatively small number of participants suggests large treatment effect sizes (the magnitude of the treatment) with limited variability of test scores (participants had similar gains) following neurofeedback. One potential confound includes that participants’ IQ fell in the average range, which may not be representative of some persons with ASD. The researchers reported, however, a wide range of IQ scores in the experimental and control groups (73-111 and 82-199, respectively).

Coming Soon: PT 2 of this research investigates whether treatment gains realized in the current study were maintained 1 year later.

Editorial Update:
Part 2 of this article can now be found here.
Mirjam Kouijzer’s (the principal investigator of this research) response to our story is here.

2 Responses to Neurofeedback For Autistic Spectrum Disorders: Promising Results In A Small Sample

This is a technical discussion that may interest only neurotherapists. Others may have trouble following this discussion:

The protocol used is somewhat unclear to me after a reread of this study. I do not believe now that a 2 channel protocol was used as I originally reported. The authors described electrodes placements at C3/C4 and A1, with A1 being a reference electrode. There is no mention of a A2, which is typically required in a 2 channel hook up. This means that C3 must have been a ground channel. I have never used a 10/20 location as ground location, but this does not mean that it cannot be done. Thus, I believe that the researchers used a single channel protocol at C4. I plan to contact them for elaboration. CFisher

Posted on behalf of Mirjam Kouijzer (lead author of the research currently being discussed):

Investigating effects of neurofeedback for autism spectrum disorders (ASD) is a relatively new field of research. Our first results were recently published in a paper that was reviewed by Christopher Fisher.

Furthermore, a second paper investigating the long-term results of this treatment is now in press and expected soon. These positive results have given incentive for further studying the effects of neurofeedback in ASD. We are currently working on more extensive studies with larger samples to be able to draw more conclusions about the effects of neurofeedback for children with ASD and the working mechanisms that underlie these results. I am very happy to notice that neurofeedback is being discussed and of interest in a growing number of people. In order to be accepted as a full-fledged treatment next to behavioral therapy and medication, replications of the effects we found and additional studies with improved design to control for unspecific factors are needed.

In addition to the summary that was given here, I would like to point to the results we found in the session data. This data comprises brain wave activity at the location where the electrode was placed during treatment, i.e. C4. At this location, participants were instructed to inhibit slow wave (theta) activity while enhancing faster brain waves (low beta or SMR) for 40 sessions. 65% of the participants showed a significant decrease in theta power and a significant increase in low beta power over 40 sessions. These data indicate that children with ASD are indeed able to act upon their brain wave activity. Interestingly, other studies examining effects of neurofeedback in other populations also point to 60-70% success rates.

While reading Fisher’s comment I noticed some confusion about the protocol used in the study. As I mentioned before, treatment occurred at C4, that is, at the right hemisphere central location. The paper described electrode placement at C3 and C4, but feedback came only from C4. C3 was used only for monitoring brain wave activity over the left hemisphere. We found that neurofeedback training at C4 affects activation over both hemispheres. I hope this explanation clarifies the questions about the exact protocol that was used.